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10.18632/oncotarget.7272 http://scihub22266oqcxt.onion/10.18632/oncotarget.7272 C4905494!4905494!26871465     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (10): 11567-79 Nephropedia Template TP {{tp|p=26871465|t=2016. HIF-3?1 promotes colorectal tumor cell growth by activation of JAK-STAT3 signaling |pdf=|usr=}}{{26871465}} gab.com Text HIF-3 1 promotes colorectal tumor cell growth by activation of JAK-STAT3 signaling JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26871465 #FOAvip Hypoxic environment is critical in colorectal cancer (CRC) development. Most studies have mainly focused on hypoxia-inducible factor (HIF)-1? and HIF-2? as the major hypoxic transcription factors in CRC development and progression. However, the role of HIF-3? in CRC is not clear. Here we found that HIF-3? protein was increased in colorectal tumors from both mouse models and human patients. Moreover, increased HIF-3? expression was correlated with decreased survival. Overexpression of a long isoform of HIF-3?, HIF-3?1, increased cell growth in two CRC cell lines. Surprisingly, overexpressed HIF-3?1 was localized to the cytosol and increased phosphorylated signal transducer and activator of transcription 3 (p-STAT3). STAT3 inhibition effectively reduced p-STAT3 levels and cell growth induced by HIF-3?1. The activation of p-STAT3 was independent of the transcriptional activity of HIF-3?1. However, the inhibition of the upstream regulator Janus kinase (JAK) abolished HIF-3?1-induced p-STAT3 and cell growth. Together, these results demonstrated that HIF-3?1 promotes CRC cell growth by activation of the JAK-STAT3 signaling pathway through non-canonical transcription-independent mechanisms. Twit Text FOAVip HIF-3 1 promotes colorectal tumor cell growth by activation of JAK-STAT3 signaling ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26871465 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26871465 #FOAvip English Wikipedia <ref>{{Cite pmid|26871465}}</ref> HIF-3?1 promotes colorectal tumor cell growth by activation of JAK-STAT3 signaling #MMPMID26871465 Xue X; Jungles K; Onder G; Samhoun J; Gy?rffy B; Hardiman KM Oncotarget 2016[Mar]; 7 (10): 11567-79 PMID26871465show ga Hypoxic environment is critical in colorectal cancer (CRC) development. Most studies have mainly focused on hypoxia-inducible factor (HIF)-1? and HIF-2? as the major hypoxic transcription factors in CRC development and progression. However, the role of HIF-3? in CRC is not clear. Here we found that HIF-3? protein was increased in colorectal tumors from both mouse models and human patients. Moreover, increased HIF-3? expression was correlated with decreased survival. Overexpression of a long isoform of HIF-3?, HIF-3?1, increased cell growth in two CRC cell lines. Surprisingly, overexpressed HIF-3?1 was localized to the cytosol and increased phosphorylated signal transducer and activator of transcription 3 (p-STAT3). STAT3 inhibition effectively reduced p-STAT3 levels and cell growth induced by HIF-3?1. The activation of p-STAT3 was independent of the transcriptional activity of HIF-3?1. However, the inhibition of the upstream regulator Janus kinase (JAK) abolished HIF-3?1-induced p-STAT3 and cell growth. Together, these results demonstrated that HIF-3?1 promotes CRC cell growth by activation of the JAK-STAT3 signaling pathway through non-canonical transcription-independent mechanisms. äHIF-3?1 promotes colorectal tumor cell growth by activation of JAK-STA(epmc).pdf DeepDyve Pubget Overpricing